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大鼠离体灌注尾动脉对氯化钾血管收缩反应的机制:与α2-肾上腺素能受体激动剂UK14304的相互作用

Mechanisms of vasoconstrictor responses to KCl in rat isolated perfused tail arteries: interaction with the alpha 2-adrenoceptor agonist UK14304.

作者信息

Xiao X H, Rand M J

机构信息

Department of Pharmacology, University of Melbourne, Victoria, Australia.

出版信息

Eur J Pharmacol. 1991 Apr 17;196(2):133-6. doi: 10.1016/0014-2999(91)90418-p.

Abstract

The vasoconstriction in rat tail arteries during exposure to 56 mM KCl for 2-5 min consisted of an initial sharp peak followed by a secondary plateau. Both components were reduced by the alpha 1-adrenoceptor antagonists prazosin and WB4010. In arteries from reserpine-pretreated rats, the plateau was markedly reduced and only slightly further attenuated by prazosin, however the initial peak was not reduced but was now not affected by prazosin. Thus, the response to KCl in arteries from normal rats is partly due to release of noradrenaline, and this occurs to a greater extent in the plateau than in the peak component. Addition of UK14304 during the plateau reduced the vasoconstriction in arteries from normal rats; however, in arteries from reserpine-pretreated rats there was increased vasoconstriction. These effects of UK14304 were abolished by idazoxan and were not affected by prazosin, and can be attributed to prejunctional inhibition of noradrenaline release in arteries from normal rats and postjunctional enhancement of vasoconstriction in arteries from reserpine-pretreated rats.

摘要

在暴露于56 mM氯化钾2 - 5分钟期间,大鼠尾动脉的血管收缩包括一个初始的尖峰,随后是一个继发性平台期。这两个成分都被α1 -肾上腺素能受体拮抗剂哌唑嗪和WB4010降低。在利血平预处理大鼠的动脉中,平台期明显降低,哌唑嗪仅使其略有进一步减弱,然而初始尖峰未降低,但现在不受哌唑嗪影响。因此,正常大鼠动脉对氯化钾的反应部分归因于去甲肾上腺素的释放,并且这种情况在平台期比在尖峰成分中发生的程度更大。在平台期添加UK14304可降低正常大鼠动脉的血管收缩;然而,在利血平预处理大鼠的动脉中,血管收缩增强。UK14304的这些作用被咪唑克生消除,且不受哌唑嗪影响,可归因于正常大鼠动脉中去甲肾上腺素释放的突触前抑制以及利血平预处理大鼠动脉中血管收缩的突触后增强。

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